TNFRSF18 and cancer: GITR ligation provides a co-stimulatory signal that enhances both CD4+ and CD8+ T-cell proliferation and effector functions, particularly in the setting of suboptimal TCR stimulation.[2], [3], [4], [5] In addition, co-stimulation through GITR has been shown to make naïve or effector T cells (Teffs) resistant to the suppressive effects of Tregs in vitro, and can enhance auto-reactive, allo-reactive, and anti-viral T-cell responses in vivo.[2], [6], [7], [8], [9], [10], [11], [12], [13] This makes targeting GITR a potential immunotherapeutic approach to cancer treatment.